Marc Roelke

Limitations and Late Complications of Third-Generation Automatic Cardioverter-Defibrillators

BACKGROUND This study examines the limitations and complex management problems associated with the use of tiered-therapy, implantable cardioverter-defibrillators (ICDs). METHODS AND RESULTS The study group comprises the first 154 patients undergoing implantation of tiered-therapy ICDs at our institution. Pulse generators from three different manufacturers were used. In 39 patients, a complete nonthoracotomy lead system was used. The perioperative mortality was 1.3%. Of these 154 patients, 37% experienced late postoperative problems. Twenty-one patients required system revision within 36.5 months (mean, 8.57 +/- 11.3) of surgery. Reasons for revision were spurious shocks due to electrode fractures (3) or electrode adapter malfunction (2), inadequate signal from endocardial rate-sensing electrodes (3), superior vena cava or right ventricular coil migration (5), failure to correct tachyarrhythmias due to a postimplant rise in defibrillation threshold (5), or pulse generator failure (3). One of these patients required system removal for infection after revision of an endocardial lead. A further 32 patients received inappropriate shocks for atrial fibrillation with a rapid ventricular response or sinus tachycardia. Two of these patients also received shocks for ventricular tachycardia initiated by antitachycardia pacing triggered by atrial fibrillation. Ventricular pacing for bradycardia was associated with inappropriate shocks due to excessive autogain in 2 patients. CONCLUSIONS Despite the major diagnostic and therapeutic advantages of tiered-therapy ICDs, a significant proportion of patients continue to experience hardware-related complications or receive inappropriate shocks.

Patients' Attitudes Toward Implanted Defibrillator Shocks

In addition to its beneficial effect on patient survival, the implanted cardioverter defibriliator (ICD) changes a patients life physically, socially, and psychologically. For improved patient management, it is important to understand the quality‐of‐life changes that accompany this mode of treatment. To this end, 119 patients were surveyed retrospectively and interviewed concurrently regarding their emotional, physical, and behavioral responses to ICD shocks and to the device itself. Most (55%) correctly estimated the total number of shocks they had received within a 10% margin. They found the shocks severe, 79% assigning a score between 3 and 5 on a scale of 1–5. Common descriptions of the shock sensation were a blow to the body or a spasm causing the entire body to jump. Most patients tolerated the shocks as life saving, but 23% dreaded shocks and 5% even said they would rather be without the ICD and take their chances. After a shock, 50% of patients called their physician and 42% continued their daily routine. Thirty percent went to a hospital emergency room or called a rescue service. Sixty‐five percent had no preshock prodromes. Fifty‐four percent were interested in the programmable option of a warning signal prior to a shock, while 31 % preferred no warning. Of the 74% who were advised not to drive after implantation, 29% drove anyway. Five patients were shocked while driving with no resulting accidents. We conclude that most patients find ICD shocks moderately uncomfortable, but they tolerate them because of the lifesaving protection provided by the device.

Subclavian Crush Syndrome Complicating Transvenous Cardioverter Defibrillator Systems

Subclavian crush syndrome, described with pacemaker leads implanted via subclavian puncture, may occur when conductor fractures and insulation breaches develop by compression of a lead between the first rib and clavicle. We reviewed our experience in 164 patients who underwent intended implantation of transvenous defibrillator systems to determine the clinical relevance of subclavian crush syndrome in defibrillator patients. Venous access was obtained via subclavian puncture in 114 patients (70%) and via cephalic cut‐down in 50 patients (30%). Nonthoracotomy lead systems, with or without subcutaneous patch, were successfully implanted in 131 of 164 patients (79.9%). Thoracotomy was required in 32 patients (19.5%) and subxiphoid patch in 1 patient (0.6%). Over a mean of 12.9 months (range 1–62 months), 3 patients (1.8%) required revision of the rate sensing lead/coil or superior vena cava coil after development of lead compression fractures in the region of the clavicle and first rib. In all 3 patients the leads had been implanted via subclavian puncture (2.6% of patients in whom the subclavian technique was utilized). Two patients presented with spurious shocks. One patient was asymptomatic. Conclusions: When venous access is obtained via subclavian puncture, subclavian crush syndrome may develop in patients with transvenous defibrillator systems. Patients may be asymptomatic and lead fractures may go unrecognized. When implanting transvenous defibrillator systems, strong consideration should be given to obtaining venous access primarily via the cephalic cut‐down technique.

Analysis of the initiation of spontaneous monomorphic ventricular tachycardia by stored intracardiac electrograms.

OBJECTIVES This study was designed to analyze stored intracardiac electrograms generated during spontaneous monomorphic ventricular tachycardia to examine the possible mechanisms responsible for the initiation of ventricular tachycardia in a group of postinfarction patients. BACKGROUND Implantable cardioverter-defibrillators capable of storing electrograms during an arrhythmic event provide an intracardiac electrogram analog to Holter ambulatory electrocardiographic monitoring. Such electrograms are of value in arrhythmia diagnosis and in determining the appropriateness of implantable cardioverter-defibrillator therapy and may aid in understanding the initiation of ventricular arrhythmias. METHODS We studied 73 stored electrograms in 22 postinfarction patients with spontaneous monomorphic ventricular tachycardia. Premature depolarizations before tachycardia were classified by morphology and number. Electrogram morphology was compared with the morphology of the baseline rhythm and ventricular tachycardia. Prematurity was assessed by the coupling interval and a calculated prematurity ratio. RESULTS During baseline rhythm, ectopic activity was present in 30 (41%) of 73 stored episodes. Ventricular tachycardia was preceded by a short-long-short sequence in 14% of episodes and by a rapid ventricular rhythm in 5.5% of episodes. The onset of ventricular tachycardia was marked by single premature depolarizations in 33 episodes (45%), by pairs in 16 (22%) and by multiple complexes in 24 (33%). Morphology was similar to that of the ensuing tachycardia in 35 episodes (48%). The mean coupling interval was 364 ms, and the mean prematurity ratio was 0.56. In all 10 episodes (14%) where the prematurity ratio was < 0.40, a short-long-short sequence was responsible. When classified by morphology, the mean prematurity ratio of depolarizations dissimilar to ventricular tachycardia (0.53) was significantly less than that of the morphologically similar group (0.60, p = 0.035). CONCLUSIONS In this select group of postinfarction patients with recurrent sustained monomorphic ventricular tachycardia treated with implantable cardioverter-defibrillators, ventricular tachycardia was most often preceded by late-coupled premature depolarizations. Not infrequently, a short-long-short sequence occurred before tachycardia. Premature depolarizations with a morphology different from that of the tachycardia occurred earlier in the cardiac cycle than did those with a morphology similar to that of the tachycardia. These findings may reflect different mechanisms of ventricular tachycardia initiation.

The treatment of patients with infected implantable cardioverter-defibrillator systems

OBJECTIVE The purpose of this study was to evaluate the treatment of patients with infected implantable cardioverter-defibrillator systems. METHODS Retrospective analysis was done of the cases of 21 patients treated for implantable cardioverter-defibrillator infection during an 11-year period. RESULTS Of 723 cardioverter-defibrillator implantations (550 primary implants, 173 replacements), nine (1.2%) were complicated by early postoperative device-related infections. Late infections developed in two patients 19 and 22 months, respectively, after implantation. Ten other patients were transferred to our institution for treatment of cardioverter-defibrillator infection. The time from implantation to overt infection was 2.2 +/- 1.3 months, excluding the two late infections. The responsible organisms were Staphylococcus aureus (9), Staphylococcus epidermidis (6), Streptococcus hemolyticus (1), gram-negative bacteria (3), Candida albicans (1), and Corynebacterium (1). All patients were treated with intravenous antibiotic drugs. Total system removal was done in 15 patients and partial removal in 2; in 4, the cardioverter-defibrillator system was not explanted. There were no perioperative deaths. A new implantable cardioverter-defibrillator system was reimplanted in 7 patients after 2 to 6 weeks of antibiotic therapy. Ten patients were treated without reimplantation (2 arrhythmia operation, 8 antiarrhythmic drugs). Four patients (3 patients without explantation and 1 with partial system removal) were treated with maintenance long-term antibiotic therapy. During a mean follow-up of 21 +/- 2.8 months, no patient had clinical recurrence of infection. One patient treated with antiarrhythmic drugs without system reimplantation died suddenly. CONCLUSIONS Infections that involve implantable cardioverter-defibrillator systems can be safely managed by removing the entire system with reimplantation after intravenous antibiotic therapy. In selected patients in whom the risk for system explantation is high and anticipated life expectancy is short, long-term antibiotic therapy to suppress low-virulence infections may represent an acceptable alternative.

Reduction of RV pacing by continuous optimization of the AV interval

Background: In patients requiring permanent pacing, preservation of intrinsic ventricular activation is preferred whenever possible. The Search AV+ (SAV+) algorithm in Medtronic EnPulse™ dual‐chamber pacemakers can increase atrioventricular (AV) intervals to 320 ms in patients with intact or intermittent AV conduction. This prospective, multicenter study compared the percentage of ventricular pacing with and without AV interval extension.

A prospective randomized trial of defibrillation thresholds from the right ventricular outflow tract and the right ventricular apex.

Background: Right ventricular outflow tract (RVOT) pacing has been suggested to improve hemodynamics and to help prevent pacing‐induced cardiomyopathy. Pacing from the RVOT is feasible and equivalent in terms of sensing and stimulation threshold. However, physicians have been reluctant to use RVOT pacing because of concerns that defibrillation efficacy might be adversely affected. To date, there have been no randomized‐controlled trials published comparing the defibrillation threshold in leads implanted in the RVOT and the right ventricular apex (RVA).

Asystole after exercise in healthy persons

Exercise-related syncope is infrequent in healthy persons, although vasodepressor syncope reproduced by positive head-up tilt testing has been reported in small series of healthy persons [1] and athletes [2] with syncope after exercise. Whether vasodepressor syncope may also occur during exercise is controversial and is now an issue of public debate [3]. Asystole after exercise is an extremely rare finding in healthy persons, and single cases without clear proof of the underlying mechanisms have been reported during the past 20 years [4-7]. We describe three patients with recurrent exercise-related syncope in whom prolonged asystole after exercise was documented. Positive head-up tilt table testing in all three patients suggested neurocardiogenic syncope as the underlying mechanism. Case Reports Patient 1 A 34-year-old man had atypical chest pain and a history of multiple episodes of syncope and presyncope, all related to physical stress. Two syncopal episodes occurred immediately after weight lifting. Submaximal exercise test results did not indicate ischemia. However, 1.5 minutes into recovery, the patient developed sudden asystole (lasting for 32 seconds) with rare ventricular escape beats (Figure 1). This resulted in respiratory arrest, and chest massage was initiated by the supervising physician; the patient recovered just before being intubated. Fifteen months later, he had another syncopal episode while walking into the bathroom at night. A chest radiograph, a 12-lead electrocardiogram, 24-hour Holter monitoring, and an echocardiogram all yielded normal test results. Head-up tilt testing was done, and, after 4 minutes in the upright position, the patient became abruptly asystolic for 23 seconds without previous symptoms or hypotension (blood pressure before asystole, 123/92 mm Hg; heart rate, 92 beats per minute). He lost consciousness and made a slow recovery after returning to the supine position. With avoidance of strenuous exercise, the patient has remained free of syncope without drug or pacemaker therapy during 9 months of follow-up surveillance. Figure 1. The rhythm strip starts 1. Patient 2 A 22-year-old man had four episodes of syncope in a 1-year period, all occurring during or immediately after playing basketball. During warm-up before a game, he had a syncopal spell while standing still after running. He reported several similar episodes that he shortened by lying supine. Echocardiography showed moderate concentric left ventricular hypertrophy without evidence of outflow tract obstruction and showed a left ventricular ejection fraction of 75%. The surface electrocardiogram was consistent with left ventricular hypertrophy, but arterial blood pressure measurements were repeatedly normal. One minute after maximal exercise testing, he developed a sudden onset of bradycardia associated with near syncope, and several 4- to 6-second periods of asystole were documented followed by sinus bradycardia with first-degree atrioventricular block. Thallium imaging results were normal. The results of a comprehensive electrophysiologic study were also normal. Ten minutes into head-up tilt table testing, the patient had vasodepressor syncope (systolic blood pressure, 60 mm Hg) accompanied by mild bradycardia (43 beats per minute). A repeated exercise test, with a scopolamine patch in place, showed normal results. Scopolamine was prescribed but was subsequently discontinued because of side effects. The patient has taken oral disopyramide for 38 months and has had an uneventful course during this time; he continues to play basketball. Patient 3 A 35-year-old man had two presyncopal episodes, one immediately after strenuous exercise and the second after fighting a fire. His clinical evaluation was unremarkable. Echocardiographic results showed mild mitral valve prolapse without mitral regurgitation and showed normal left ventricular function. Exercise radionuclide ventriculographic results were normal. Eight minutes into recovery, while seated, the patient had sudden asystole for 15 seconds with a brief loss of consciousness followed by a slow sinus recovery at a rate of 10 to 20 beats per minute. Respiratory arrest occurred, but cardiac and respiratory function returned spontaneously. Comprehensive electrophysiologic study results were entirely normal. Head-up tilt table testing at baseline was unremarkable, but repeated testing using intravenous isoproterenol (0.025 g/kg per minute) provoked vasodepressor syncope (blood pressure, 80/60 mm Hg) with relative bradycardia (heart rate decrease from 120 to 64 beats per minute) after 15 minutes in the upright position. The patient started receiving atenolol (25 mg per day); repeated head-up tilt test and exercise test results (maximal heart rate, 148 beats per minute; Bruce stage 8) were normal. While receiving atenolol, the patient has remained free of recurrent syncope after 9 months of follow-up. Discussion Single cases of asystole after exercise have been described previously, but the underlying mechanisms have been uncertain [4-7]. Our findings of positive head-up tilt test results in all three patients suggest that a variant of neurocardiogenic syncope may be one mechanism of asystole after exercise, but additional abnormalities in the autonomic control of the cardiovascular system seem to be involved. Blood pressure control at rest and also in response to changing posture is mainly regulated through the baroreceptor reflex [8]. The response to exercise involves additional mechanisms [9] (such as increased sympathetic activity) that have been partly ascribed to the so-called metaboreflex activated by metabolites from ischemic muscles [10, 11]. After exercise, the heart rate decreases to baseline, although the blood pressure remains increased, despite continuing activation of this reflex by ongoing muscle ischemia. This phenomenon has been attributed to an exercise-induced up-regulation of the parasympathetic efferent tone, which, in the period after exercise, selectively depresses the heart rate without affecting the vascular bed and blood pressure [9, 11]. The mechanisms provoking neurocardiogenic syncope are probably initiated by a progressive decrease in venous return in the upright position, which is responsible for maximal stimulation of the sympathetic system. Echocardiographic studies have documented a progressive decrease in end-diastolic and end-systolic volumes during head-up tilt table testing, with a maximal increase in fractional shortening before syncope [12]. The strong sympathetic drive in the setting of a relatively empty heart leads to vigorous myocardial contraction, which, in susceptible persons, activates mechanoreceptors in the left ventricular wall (C-fibers) and causes a profound response of the afferent vagal nerve [13]. This vagal stimulus may trigger a sudden withdrawal of the neural efferent sympathetic activity (negative feedback loop) and may increase the efferent parasympathetic tone with subsequent vasodilation and progressive hypotension [14]. Because arterial hypotension usually precedes bradycardia, inactivation of the sympathetic efferent tone and consequent vasodilation may be the primary mechanism of syncope [15]. Bradycardia and asystole, as markers of the increased parasympathetic tone, play only a secondary role in most patients with vasodepressor syncope. This view is further supported by the fact that, in most patients, hypotension and syncope cannot be avoided by atrioventricular sequential pacing [15]. Infrequently, however, cardioinhibition leading to profound bradycardia or asystole may be the dominant mechanism responsible for symptoms. In our patients, syncope and asystole typically occurred in the recovery period of exercise, when venous return was diminished (sitting position). The findings of positive results from head-up tilt testing suggest that all three patients had a low threshold to trigger an abnormal afferent parasympathetic response to decreased venous return, suggesting that venous pooling after exercise may have been one of the mechanisms triggering their asystole. However, the long latency between maximal activation of the mechanoreceptors (peak exercise) and the onset of syncope during late recovery in one of our patients (8 minutes after exercise) and in another of the previously reported patients (10 minutes after exercise) suggests that other mechanisms, such as inappropriate control of the sympathetic tone after exercise (for example, diminished sympathetic response to muscle ischemia after exercise), may play an additional role in some patients. Based on these patients and the current understanding of neurocardiogenic syncope, it appears that asystole after exercise in otherwise healthy persons may represent a variant of this syndrome, in which the effect of increased efferent parasympathetic tone predominates over the effect of sympathetic withdrawal. The optimal management of patients with vasodepressor syncope is unknown. In theory, if initiation of the vasodepressor reflex can be prevented, the hypotension and bradycardia that follow its activation should be eliminated. Accordingly, therapy is generally directed at the underlying mechanisms rather than at the outcome. Although several drugs (including -blockers [16], disopyramide [17], and scopolamine [18]) have been used, no consensus exists about whether drug therapy or implantation of pacemakers is beneficial in treating patients with this condition [19].

Laser extraction of entrapped leads.

Parsonnet, V., et al.: Laser Extraction of Entrapped Leads. Removing entrapped pacing and defibrillator leads has been greatly simplified by making use of the excimer laser extractor. Sixty‐two leads were successfully removed, although where appropriate, portions of the lead remained in place in 10 cases. There were two serious complications, one tear of the superior vena cava during an ICD extraction and one tear of the atrium during an atrial lead extraction. Both were controlled successfully through emergency sternotomy. Although extracting entrapped leads has been much simplified by making use of the laser extractor, the process is not free of serious complications. Those involved in explanting leads should be aware of the outcomes and be prepared for emergent management.

Submammary Pacemaker Implantation: A Unique Tunneling Technique

Submaminary pacemaker implantation offers women a cosmetically acceptable alternative to the standard pectoral implant. We present a novel method of submammary implantation performed on ten women aged 13–54 years. The lead electrodes are tunneled from the infraclavicular to the inframammary incision using a long needle, guidewire, and introducers/dilators in a manner analogous to the retained guidewire technique used for standard lead insertion. The procedure can generally be performed under local anesthesia. All patients tolerated the procedure well without acute complications. Over 2‐ to 23‐month follow‐up, there were no lead dislodgments. No patients developed mastitis or incisional complications, and all have been extremely satisfied with the cosmetic results. With proper technique, submammary pacemaker implantation can be performed under local anesthesia with minimal patient discomfort and optimal cosmesis.